Regional spinal cord blood flow (rSCBF) in gray matter and its response to CO2 inhalation were estimated in awake rats at three spinal levels by the hydrogen clearance method and 14C-antipyrine autoradiography. Regional blood flow levels obtained by two methods were well correlated. The gray matter rSCBF values of T-11, T-13 and L-2 levels measured by the hydrogen clearance method were 35.9±3.2, 45.0±3.5 and 46.0±5.2 ml/min/100 g, respectively, and those measured by 14C-antipyrine autoradiography were between 42.2 and 51.3 ml/min/ 100 g. The rSCBF values in the thoracic gray matter were somewhat lower than those in the lumbar enlargement. The differences of rSCBF values with respect to the spinal levels were small in the white matter (20.7-22.9 ml/min/ 100 g). By CO2 gas inhalation the rSCBF increased linearly in proportion to PaCO2 increase as long as PaCO2 was below 80-90 mmHg. The effect of CO2 inhalation on rSCBF was expressed as “percent increase over basal flow against PaCO2 increase” [ΔrSCBF/ΔPaCO2/rSCBF(PaCO2=35 mmHg)×100], and the values of T-11, T-13 and L-2 levels were 6.9±0.9, 4.9±1.1 and 7.0±0.4 %/mmHg, respectively.
An experimental model of the spinal epidural neoplasm was produced in rats by injecting Walker 256 carcinoma cell suspension anterior to the T-12/13 vertebral body. Using this animal model, regional spinal cord blood flow (rSCBF) and its response to CO2 inhalation (CO2 R) were estimated by 14C-antipyrine autoradiography and the hydrogen clearance method. In the early stage of weakness of the hind limbs, axonal swelling and edema of the white matter were revealed by histopathological examination, while both rSCBF and CO2-R remained normal. In the middle stage of weakness, the tumor invaded the spinal canal and compressed the spinal cord epidurally, and edema of white matter progressed although the gray matter was scarcely affected. The rSCBF decreased gradually at the compressed and caudal levels. Disturbance of CO2-R was also noted at the compressed and caudal levels, and appeared to preceed the rSCBF decrease. The disturbances of rSCBF and CO2-R were remarkable at the compressed level than at the caudal level. No disturbances were observed at the rostral level. In the end stage of weakness, disturbances of rSCBF and CO2-R progressed rapidly and microangiography revealed obstruction of the vertebral venous plexus at the level of compression, while the greater vessels (radicular arteries, anterior spinal artery, posterior spinal arteries and posterior median vein) were patent even in this stage. From the data collected, the pathophysiology in the spinal epidural neoplasm is considered as follows : 1) the vertebral venous plexus is stenosed or obstructed by the epidural tumor in the early stage of weakness and vasogenic edema starts in the spinal cord; 2) as the tumor grows, mechanical compression of the spinal cord occurs in addition to obstruction of the vertebral venous plexus, and the edema progresses further; and 3) rSCBF decreases rapidly to the critical flow level in the end stage and the cord function becomes irreversible.
In experimental cerebral infarction models of dogs, 10-15 ml of 20% Fluosol DA was used to estimate its effectiveness on the basis of improvement in microcirculation and changes in the size of infarction lesions. Comparative studies were also performed on four other groups consisting of the control (nonmedicated group), mannitol group (2 g/kg), low-molecular dextran group (10 ml/kg) and mannitol +Fluosol DA group. Fluosol DA was effective even when used alone, but its combination with mannitol proved the most effective. It was concluded that Fluosol DA should be an effective medicine for acute cerebral infarction.
In the previous paper (Part I), an experimental model of hydrocephalus produced by inoculating cells derived from a human brain tumor into the brain of mice was described, with emphasis on the method of preparation and histological findings. In this paper (Part II), hydrocephalus produced by inoculated cells such as RGC-6 cells and Hela-S3 cells into the brain of mice is described. Hydrocephalus was not produced by the inoculation of culture medium or dead cells. However, homogenized Hela-S3 cells produced hydrocephalus. The causal genesis is still unknown.
An electron microscopic study of 15 cases of prolactin-producing pituitary adenomas removed by operations was performed. The cases consisted of 14 females and one male, and all of the female patients manifested galactorrhea. The resting serum level of prolactin ranged from 200 to 2, 650 ng/ml, which responded well to intravenous TRH, increasing to 7, 290 ng/ml. Out of 15 patients, nine harbored intrasellar microadenoma, and the others harbored large tumor masses showing suprasellar extension. The age distribution was from 20 to 70 years, with an average of 25.7 years for the microadenoma-group and an average of 42.7 years for the large tumor-group. Electron microscopic observations of adenomas obtained from 11 patients who had not received bromocriptine revealed adenoma tissue composed of polyhedral adenoma cells. The large central nuclei had irregular outlines. Endoplasmic reticulum and Golgi apparatus were well developed. In two cases, the adenoma cells had abundant microvilli. In the cytoplasms, there were characteristic pleomorphic secretory granules measuring up to 450 my in the longest dimension, which were considered to be prolactin granules. There were also round secretory granules, measuring 100-300 my in diameter, intermingling with the pleomorphic secretory granules. These secretory granules were electrodense, and had a limiting membrane. Exocytosis of the secretory granules was frequently encountered. Cilia and junctional complexes were occasionally observed, but intraadenomatous calcification and intracytoplasmic accumulation of fine filaments were rarely seen. These findings suggested an increased cellular activity of the adenoma cells in hormone synthesis and release. No difference in the fine structures was noticed between the microadenomas and large tumors. Bromocriptine was given preoperatively in three cases, and the serum prolactin levels were markedly reduced. In two cases, the secretory granules were increased in number and accumulated within the cytoplasm. Most of the granules were round in shape, measuring 100-400 mμ in diameter. These were fewer pleomorphic secretory granules, measuring up to 600 mμ in diameter. No exocytosis of the secretory granules was observed. In the other case, the secretory granules decreased in number and frequently were hardly observed. There were numerous multivesicular structures in the cytoplasm. These findings in bromocriptine-treated cases suggested that the drug acted to reduce the cellular activity in both hormone synthesis and release. The remaining case clinically showed the galactorrhea-amenorrhea syndrome, but an electron microscopic study disclosed a fine structure similar to that of the non-functioning adenoma. The adenoma tissue was composed of polygonal adenoma cells, which contained a few round secretory granules measuring 100-200mμ in iameter. The granules were covered with a limiting membrane, leaving a clear halo between the membrane and the dense core. The ultrastructural findings in this particular case suggested an interference inproduction, release and transport of PIF by suprasellar extension of theadenoma. Electron microscopy is an essential tool in establishing the final diagnosis of prolactin-producing adenomas of the pituitary.
Surgical treatments to increase cerebral blood flow in moyamoya disease such as STA-MCA anastomosis, encephalo-myo-synangiosis (EMS), encephalo-duro-arterio-synangiosis (EDAS) and omentum transplantation have been reported. Thirteen EMS and three EMS with STA-MCA anastomosis were performed on 12 patients with moyamoya disease, and the postoperative angiograms were analyzed. EMS was followed by recovery of paresis, disappearance of involuntary movement and disappearance or decrease of TIA. Half of the patients showed some recovery of the disturbance of intelligence. Younger patients recovered better than the adult cases. Complications after EMS were a case of transient dysarthria and dysphasia, a case of transient focal convulsvie seizure, a case of subcutaneous wound infection and a chronic subdural hematoma. No more severe side effects of EMS were seen. Selective external carotid angiograms performed over three months after EMS showed extensive filling of the cortical branches of the middle cerebral artery via the fine vascular networks fed by enlarged deep temporal arteries. New anastomoses between the cortical arteries and the middle meningeal artery were demonstrated in four cases. Moyamoya vessels in the region of the basal ganglia decreased in most cases after EMS. Modified EMS in which only the deep sheath of the temporal muscle was used for covering the cerebral surface had a similar effect. This method had less cosmetic disadvantage and less compression of the brain by blocking of the planted muscle. The postoperative external carotid angiograms disclosed multiple irregular narrowing, stenosis and occlusion of the cortical branches of the middle cerebral artery with fine revascularization in the distal region away from the site of EMS. These findings suggested that the primary occlusive process had spread over the cortical branches of the middle cerebral artery. Surgical treatments such as EMS and STA-MCA anastomosis should be tried on patients with moyamoya disease, especially in (1) younger cases, (2) cases with ischemic neurological deficit and/or (3) progressive cases.
In order to investigate the clinical features and the prognosis of brain tumors in the aged, 132 cases over 60 years of age were studied from the consecutive series of 1, 793 brain tumors in the University of Tokyo Hospital (1963-1979). The incidence of brain tumors in the aged was 7.4% on the whole, while it showed a significant increase from 4.8% (1960's) to 11.5% (the latter half of 1970's). Histologically, meningiomas were the most common tumors (26%), followed by neurinomas (17%), pituitary adenomas (16%) and metastatic tumors (15%). Malignant gliomas were found more frequently than benign ones. There were more meningiomas as age advanced. The proportion and the number of meningioma cases has obviously increased in recent years when CT scanners became available. Symptoms of intracranial hypertention were found less frequently in aged patients although they were still common in cases of glioblastomas. The duration from onset to surgery was relatively long, especially in cases of neurinomas and pituitary adenomas. Two cases of astrocytomas belonged to the category of silent gliomas. Overall operative mortality rate was 10.6%, while it showed a marked decrease to 4.7% in the 1970's. Five-year survival rates were as follows: meningiomas (58%), pituitary adenomas (70%), neurinomas (80%), glioblastomas (20%) and astrocytomas (25%). As for functional prognoses, 30% of the patients showed poor states on ADL, mostly because of residual psychic disorders.
In 1938, Cushing and Eisenhardt first described one case of meningotheliomatous meningioma with intracellular “hyaline inclusion”, later named pseudopsammoma bodies by Kepes. The meningiomas with pseudopsammoma bodies belong to a very rare entity, and were described in only five previous reports. The present case was a 41-year-old female with a short history of convulsive disorder. Precontrast CT scan disclosed a high density mass in the right sphenoidal ridge and a contrast study showed marked enhancement. Neuroradiological examination including right carotid angiography demonstrated findings compatible with a sphenoidal ridge meningioma. A front-temporal craniotomy was performed and the mass was removed totally. Microscopic examination disclosed that the tumor was composed of whorls of meningotheliomatous cells and that many tumor cells contained intracellular eosinophilic and round or oval shaped inclusions. Histochemically, the inclusions were PAS-positive, diastase and neuraminidase resistant, and conjugated with concanvalin A (Con A). These staining reactions suggested that the inclusions were composed of glycoprotein, as previously reported by Kepes and others, and that they had mannose or glucose as receptors of Con A. Macrophages were seen to infiltrate around tumor cell clusters, and showed phagocytosis of the inclusion bodies. Some metachromasia was also observed. Electron microscopically, these substances were located in the intracellular spaces lined by microvilli, and numerous well-developed desmosomes were found at the intercellular junctions. These characteristics are quite similar to those of pleural mesothelioma, and suggested some relationship between normal meningeal cells and mesothelial cells in oncogenetic and anatomic aspects. In earlier reports, the substances were said to be secretory products and a possibility of meningioma cell differentiation to secretory cells was postulated. The results of the present study with Con A staining strongly support this opinion.
A 20-year-old woman was admitted in November, 1978 because of left proptosis, which had progressed slowly since September, 1977. Her eye ball movement was normal and no other neurological dificits were noted. Plain skull roentgenograms suggested an osteogenic tumor of the left medial supraorbital region. Left carotid angiography showed hypertrophied ethmoidal branches of the ophthalmic artery. Bifrontal craniotomy was performed. The left orbital bone was separated from the dura mater and removed. An encapsulated ovoid tumor (3.5×3.5×4.0 cm) appeared under the thinned and expanded orbital bone. The main mass was situated in the left ethmoidal sinus. The tumor, which was separated from the dura mater and periorbita by the membranous bone, was removed piece by piece, totally. Postoperatively, the left proptosis decreased but a slight disturbance of the left eye ball movement occurred. Typical psammomatous meningioma was noted microscopically. She was discharged in December, 1978 with slight disturbance of the left eye ball movement and mild proptosis. She had no symptoms in September 1980. A total of 60 cases of primary ectopic meningioma were reviewed from the literature.
Two cases of intracranial hemorrhage due to the congenital deficiency of coagulation factor XIII were experienced. The first case was a 25-year-old man with an intracerebral hemorrhage in the right parieto-occipital region and was treated conservatively by hematological replacement therapy. The second case was a 30-year-old woman with an intracerebral hemorrhage in the parietal region which was surgically treated. Both cases were completely cured. Since Duckert described the first case of the congenital deficiency of coagulation factor XIII in 1960, 93 cases have been reported in the literature. The clinical picture of the intracranial hemorrhage based upon factor XIII dificiency is characterized by a tendency of spontaneous rebleeding 48 hours to several days after temporary cessation of bleeding. Therefore, no case of surgical treatment has been reported yet. The second case showed unconsciousness and intracranial hypertension and was treated by craniotomy and removal of the intracerebral hematoma. Replacement therapy with a factor XIII preparation was given before, during and after the operation. No side effects of the factor XIII replacement therapy were noted. Surgical therapy for the congenital deficiency of coagulation factor XIII might be safe if the patient is controlled by hematological replacement therapy.
A 41-year-old woman with a traumatic arteriovenous fistula of the middle meningeal artery and a sagittal epidural hematoma was reported with a review of the literature. The arteriovenous fistula was confirmed by angiography 7 and 24 days after trauma and was no longer demonstrable in a follow-up examination after 5 months. Forty-two traumatic middle meningeal arteriovenous fistulas including the author's case have already been reported throughout the world. Twenty-five of them (60%) were accompanied by epidural hematoma and seven of them(17%) closed spontaneously. It is sometimes difficult to locate extravasated contrast material in connection with the middle meningeal vein. Characteristic features of the fistulas were classified into the following five groups from operative and histological findings: 1) middle meningeal artery—middle meningeal vein fistula; 2) middle meningeal artery—diploic vein fistula; 3) pseudoaneurysm, concomitant with fistula; 4) torn dura, concomitant with fistula; and 5) organized epidural hematoma or thick dura with abnormal vessels. The high percentage of accompanying epidural hematoma, rapid granulation of epidural hematoma with early formation of vessels, pseudoaneurysms and tunnels in some epidural hematoma, intradural hemorrhage, and cases of late appearance of the fistula indicate that not only simultaneous injury of the middle meningeal artery and vein or diploic vein but also epidural hematoma and dural injury seem to be important in the formation of traumatic middle meningeal arteriovenous fistulas. Spontaneous closure of the fistula found in seven of the 42 cases is thought to be caused by thrombosis in abnormal vessels of the dura. The mechanism of spontaneous closure of the fistula in the author's case is thought to be as follows: sagittal epidural hematoma forced shunted venous blood to flow to the sphenoparietal sinus, but this retrograde flow resumed its original direction to the superior sagittal sinus after spontaneous reduction of the hematoma. A thrombus was formed in the stagnant middle meningeal vein inferior to the fistula and extended into the fistula orifice.